From the Executive Director

Bipolar Disorder – Missing the Point!

A recent study on bipolar disorder published at the International Journal of Epidemiology has problems. The biggest problem is it is not asking the most important question: How is bipolar disorder related to the desire and ability of people to live the lives they want to live? Bipolar disorder is a state of being characterized by certain subjective feelings and certain behaviors. If we assume that human beings are organisms which want to live their lives in enjoyable, satisfying ways, what does this state of being have to do with their ability or inability to do that?

The study is being done with apparent ignorance of the fact that human beings are meaning-making, desiring organisms who want to live their lives in certain ways and who, if they are unable to do so, are going to experience the states of being associated with all of the mental illness diagnoses. The study is missing its proper context. It is hanging in a kind of limbo. In the absence of a proper context, it is unlikely to be very useful to human beings.

I’m making an assumption here. I need to explicate it. I am assuming that human beings want to live enjoyable, satisfying lives. I’m also assuming that, in order to live satisfying and enjoyable lives, the great majority of human beings will have to be able to love the way in which they want to love and work (express themselves) in the way in which they want to express themselves. In the words of the positive psychologists, they will have to use the best part of themselves in the interest of something larger than themselves, have positive relationships with others and experience competence, achievement and mastery.

What evidence is there for these assumptions? What do human beings want in their lives? What are the roots of happiness? What are the ingredients of human well-being? What are the components of health? What are some of the factors with which health is associated?

I don’t have the answers to these questions. But I think these are the questions that need to be asked.

How does this relate to this study? This study is gathering information about people who have been diagnosed with bipolar disorder. It is comparing that information with similar information on persons who are not diagnosed with bipolar disorder or who have not been diagnosed with any psychiatric disorder. It is gathering information on the neurocognitive functioning of these people, their temperaments and personalities, their motivated behaviors, their life stories, their patterns of sleep and circadian rhythms and the outcomes and courses of their lives. It is also gathering information on biological factors – genetic components, the nature of the disease and nutrition.

But this data is being gathered in the absence of a useful context or an attempt to make meaningful sense of it. The authors say the etiology of bipolar disorder is unknown. But they don’t offer any hypotheses about what that etiology might be. And they don’t seem interested in exploring that question. It used to be that one of the psychologist’s jobs was to come up with a formulation of the case. What is going on with this person? This person is engaging in some bizarre, troubling and somewhat impairing behavior. What is the meaning of it? In what way may it be somehow functional? What can this tell us about what this person wants, how are they going about getting it and how they are reacting to the results they are achieving. These researchers aren’t asking these questions.

They also don’t seem open to the possibility that mania or depression might be somewhat functional for a person, might help a person have a useful experience or a desired experience, albeit bizarre and even impairing in some way. They are assuming that these states of beings are diseases and nothing more.

So the researchers find that there is a history of childhood trauma among the people diagnosed with bipolar disorder. They have suffered significantly more childhood trauma than the control group. But they don’t seem interested in wondering about how a history of childhood trauma would be related to the experiences and behaviors associated with bipolar disorder. Why might it be that people who have experienced childhood trauma would be subject to alternating mania and depression? How might we understand this in the context of people wanting to live satisfying and enjoyable lives? They also find that this history of childhood trauma is associated with a detrimental effect on inhibitory control and attention accuracy. This seems to fit with mania, to be somewhat of an explanation of the connection between what happened to this person as a child and being subject to manic episodes. But they don’t connect these dots.

I, for example, hypothesize that the manic episode is an attempt by an individual who has had a lot of pressure to be great and hugely successful but who is unable to do so, to experience the illusion of being great and successful. In other words it is an attempt to fake success and greatness or to have a faux experience of success and greatness.

The connections between childhood trauma and mania makes sense in this context. People who experience trauma in early life will likely have trouble managing their emotions and will have various kinds of trouble in interpersonal relationships. They will also suffer from cognitive deficits. The development of the brain in the first year of life is contingent on good attunement between mother and infant. We can assume that a child who is traumatized probably did not benefit from such attunement. So this child will suffer some cognitive and emotional deficits. Those deficits will make it difficult for him to be as successful in life as he might want to be. If a tremendous about of pressure is put on him to be successful, great, exalted, he might want to experience that kind of success and greatness. But the only way he will be able to do that is to go through a manic episode in which he can have the illusion of such greatness and success.

The researchers are not open to this connection between the states of being of mania and depression and the desire of people to live the kinds of lives they want to live and the inability to do that. Therefore, their efforts are unlikely to help human beings live the kinds of lives they want to live. Their considerations are too decontextualized from life, too divorced from what matters to human beings to be of much use.

Spooky Language!

In 2001 the late irreverent comedian George Carlin used the phrase "spooky language" to describe the wording of the 10 commandments. I do not cite Carlin in order to debase religious beliefs as he did. I think spirituality and religion can be of immense comfort and contribute to a sense of meaningful well-being for some people. I mention Carlin's comedic use of the phrase only in order to apply it to a recent study by Schmitz and colleagues entitled, "Hippocampal GABA enables inhibitory control over unwanted thoughts". This study claims that brain activity is the key to understanding a person's intrusive thoughts. But the authors of this study use spooky language in order to obfuscate and mislead about what would otherwise be a more simple, yet still difficult, non-disease matter.

This study is peppered with the same spooky language as others reported throughout academic journals and the media that make the ontological mistake of conflating human experiences with the neurochemical happenings going on during those experiences, and of using this language in a way that implies those brain happenings are pathological, while no evidence is ever presented to support that assertion.

The mental health industry is replete with this mistake because it is an inevitable result of the medical model - assuming troublesome experiences are symptoms of brain dysfunction without evidence of such. If this assumption were true, it would make sense to pay attention to brain chemistry and functioning when those experiences occur.

For instance, when a person has a brain tumor in just the right place, she might experience the world differently and act differently than without the tumor. In this situation, neurologists are helpful medical specialists who can address this problem and possibly alter brain chemistry or surgically remove the tumor in order to fix the problem.

This is similar to how a mechanic would identify a faulty car part and repair or replace it. But absent an identifiable broken brain part, this model is inappropriate when dealing with individual experiences of intrusive thoughts. People are not cars and, as far as we know, cars do not have meaningful experiences they can complain about.

Consider just a few examples of spooky language in the Schmitz study and a more simple, straightforward (non-spooky) translation in parentheses:

"Intrusive memories, hallucinations, ruminations, and persistent worries lie at the core of conditions such as post-traumatic stress disorder, schizophrenia, major depression, and anxiety." (When people complain of persistent and intrusive thoughts we say they have a disease.)

"These debilitating symptoms are widely believed to reflect, in part, the diminished engagement of the lateral prefrontal cortex to stop unwanted mental processes, a process known as inhibitory control." (When people are experiencing intrusive thoughts, we notice a part of the brain becomes less active.)

"In individuals with schizophrenia, the severity of positive symptoms, such as hallucination, increases with hippocampal hyperactivity, as indexed from abnormally elevated resting blood oxygen-level-dependent (BOLD) activity, or increased regional cerebral blood flow, blood volume, or blood glucose metabolic rate." (When the severity of intrusive thoughts increases, we notice another part of the brain becomes more active.)

"Consistent with this view, animal models of schizophrenia show that disrupting GABAergic inhibition in the hippocampus by transgenic or pharmacological manipulations reliably reproduces hippocampal hyperactivity and volume loss, along with behavioral phenomena paralleling symptoms present in this disorder." (When we disrupt the natural workings of the brain it causes problems for the owner of the brain.)

"Together, these findings suggest that a deficit of GABAergic inhibition local to the hippocampus contributes to problems controlling a spectrum of intrusive memories and thoughts, although the pathogenesis of this deficit and its specific manifestations across disorders may vary." (When people experience intrusive thoughts, an area of the brain becomes more active, but we really aren't clear on this.)

"We hypothesized that GABAergic inhibition in the hippocampus forms a critical link in a fronto-hippocampal inhibitory control pathway that suppresses unwanted thoughts." (We think two areas of the brain change in activity level when people experience intrusive thoughts.)

I could go on and on. The point is that spooky language is often used in studies like this in order to mislead the reader into thinking something that isn't true; that being, scientific medical precision about a brain disease. Despite all the medical-sounding words and phrases, there is not one bit of real evidence ever presented that intrusive thoughts have anything to do with real brain health or illness. And, by the way, if such evidence were presented, this wouldn't be a matter for psychiatry. It would be a neurological problem to be addressed by neurologists and other real medical specialists.

All this study shows is that when people are having experiences (intrusive thoughts), their brains are working. The fundamental mistake is in conflating individual experiences with the workings of the brain during those experiences, and claiming that brain activity is therefore pathological.

Perhaps an analogy would help. What if we noticed that when people are lifting weights their level of muscular contraction and innervation simultaneously react in a particular way. Would we then conclude that lifting weights is a disease? Of course not. And we wouldn't say things like, "In individuals with weight lifting disorder, the severity of positive symptoms, such as muscular contraction, increases with motor and sensory cortex hyperactivity, as indexed from abnormally elevated resting blood oxygen-level-dependent (BOLD) activity, or increased regional cerebral blood flow, blood volume, or blood glucose metabolic rate." That would be preposterous.

Muscle contraction and changes in the sensory/motor cortex is not evidence of disease and it is not the same as the human experience of lifting weights. Likewise, hippocampal and prefrontal cortex activity is not evidence of disease and it is not the same as the meaningful human experience of intrusive thoughts.

That is another matter completely.

Another Spurious Correlation? – ADHD

Are we seeing yet another spurious correlation peddled to the public as medical research? A study published at JAMA Pediatrics suggests that acetaminophen use during pregnancy causes ADHD. This study harkens back to the thalidomide controversy of the early 1960's, but instead of birth defects, the fear is that a common over-the-counter drug may disrupt fetal brain development leading to ADHD. It has been reported to the general public here and here, among other outlets, not only causing fear among parents but also continuing to perpetuate the myth that ADHD is a real disease.

This study was an analysis of over 64,000 mothers and their children from the Danish National Birth Cohort from 1996 to 2002. The researchers gathered data regarding the mothers' acetaminophen use during pregnancy and the later incidence among these mothers' offspring of problems associated with hyperactivity. The study found that the offspring of mothers who took acetaminophen during pregnancy had higher rates of these problems.

However, the difference between offspring of mothers who used acetaminophen and those who didn't was quite small. Overall, the offspring of the mothers who took acetaminophen had a 13% increased risk of scoring moderately on the Strengths and Difficulties Questionnaire. A more detailed breakdown showed the offspring of the acetaminophen mothers had: 1) a 17% increased risk of hyperactivity; 2) a 14% increased risk of conduct problems; 3) a 5% increased risk of emotional problems; and 4) a 1% increased risk of peer problems. Interestingly, there was no difference in the scores of the childrens' prosocial behaviors (this is odd since one would expect someone diagnosed with a real neurological defect to lack prosocial behaviors too).

But these are relative risk statistics. If one looks at the absolute risk, the difference becomes even more meaningless. For example, using the largest risk ratio (# 1 above - hyperactive risk), the difference in risk was a matter of 5.7% vs. 4.3%. In other words, an offspring of a mother who took acetaminophen during pregnancy had a 5.7% risk of scoring greater than a 7 on the Strengths and Difficulties Questionnaire Hyperactivity Scale, in contrast to a 4.3% risk of scoring greater than 7 by the offspring of mothers who did not take the pain reliever.

This minimal difference in risk is even more diluted when looking at the confidence intervals for the risk ratios. For two out of the four risk ratios above (emotional problems and peer problems), the 95% confidence intervals included a risk ratio of 1, which would mean there is no difference in risk between the groups of offsprings. The other two risk ratios' confidence intervals came very close to including 1.

These forgoing measures were of "ADHD-like behaviors". Well, let's see what the risk of actually being diagnosed with ADHD (actually the researchers looked at those diagnosed with hyperkinetic disorder). For the offspring of mothers who took acetaminophen, there was a 37% increased risk of being diagnosed. But again, a look at the absolute figures dilutes the practical significance of this risk ratio. The absolute risk difference in being diagnosed was around 1.5% for those mothers who took acetaminophen vs. 1% for the mothers who didn't. Hardly a matter of alarm or evidence of disease.

If there is any evidence that a drug causes fetal birth defects or neurological damage it should be taken seriously, regardless of the absolute risk. In the case of thalidomide, there was ample evidence that the toxic nature of the drug caused real defects. And, if acetaminophen is shown to cause real fetal defects, it should be treated similarly and prescribers and parents warned. But the resulting defect would not be called "ADHD" or "hyperkinetic disorder". The resulting defect would be more appropriately called a neurological disease, as would any other toxic chemical exposure, and fall under the bailiwick of the real field of medicine called neurology. The defect wouldn't be treated as ADHD and we certainly would not want to use toxic stimulant drugs to treat a real defect that was caused by another drug's toxic properties.

But this study was not looking at brain damage or defect. It was looking at the association between the incidence of acetaminophen use during pregnancy and the subsequent categorization of the offsprings' social problems using a set of checklists, not as having a neurological defect (no such defect has ever been demonstrated).

What would be a more simple interpretation of the results of this particular study? It is quite probable that parents who are more likely to resort to a pain reliever such as acetaminophen are also more keenly aware of bodily ailments, and more inclined to use chemicals to soothe those conditions instead of merely tolerating them. As these parents have children, they are also likely to transfer that concern and awareness to their children's ailments.

Therefore, when these parents wonder about their children's hyperactive behavior and other social problems that are subsumed within the diagnostic criteria of ADHD, they would be more likely to see these issues as problematic and indicative of something going wrong rather than as within the normal range of childhood behavior. They would also be more likely to consider seeking out a pediatrician or child mental health professional. Due to the pressures to diagnose in order for health insurance to reimburse a professional's time, these children would then be more likely to receive ADHD (and other) diagnoses, in addition to being the target of symptom checklists such as the Strengths and Difficulties Questionnaire. This alone could easily account for the small correlation between acetaminophen use during pregnancy and the later identification of these problems in the offspring.

The biggest problem with this study is it perpetuates the misunderstanding of ADHD as a real neurological defect, in this case one that is caused by the hormonal disruption of acetaminophen.

A New Treatment for Depression – Really?

Pay attention to language! Here is a typical example of how language is used in mental health research in order to give the impression of medicine and disease, when in fact there is nothing medical or pathological about it. Yet, it is a linguistic smoke screen that obscures the real results.

JAMA Psychiatry recently published the results of a study that claims “whole-body hyperthermia” outperformed placebo in reducing the symptoms of depression. It sounds very clinical, medical, and based on an understanding of neuroscience. The study's lead paragraphs especially set the tone and give the impression of neuroscience at work. The researchers' conclude that hyperthermia "holds promise as a safe, rapid-acting, antidepressant modality with a prolonged therapeutic benefit." Isn't there a more direct way to say this?

If you take the time to dig into the weeds and see what this study is actually saying, it is quite commonplace. It is merely proposing that increased warmth can make people feel better. Didn’t we already know this? All the talk about brain structures and pathways activated during the process of warming is irrelevant, yet it is used to make depression sound like a matter of brain pathology and "whole-body hyperthermia" as medical treatment.

Beyond the critique of language, an examination of the data further question the value of this study.

To start off, the overall difference in depression between the "whole-body hyperthermia" group and the placebo group was minimal. At 6 weeks after treatment (the longest post-treatment assessment made), the hyperthermia group’s average score on the Hamilton Depression Rating Scale was about 12 and the placebo group’s average score was about 17. A Hamilton score of 12 is within the “mild” range and 17 is within the “moderate” range. The cutoff between mild and moderate ranges is 13-14. (For now let's ignore the issue of the 86% sensitivity and 92% specificity ratings of the Hamilton).

Added to the questionable meaning of these Hamilton score differences is the fact that the confidence intervals were quite large. For example, the 6 week difference in scores was 4.27. But the 95% confidence interval for this difference was 7.94 to .61. This means there is a 95% chance that the true difference between the groups’ scores was between 7.94 and .61, and a 5% chance the difference score was outside that range. Given that the cut off score between “mild” and “moderate” depression of the Hamilton is 13-14, claiming any practically significant difference between the hyperthermia group and placebo group is dubious.

Further, it must be remembered that the above Hamilton scores are group averages and they do not sufficiently account for the individuals’ scores. The two groups' score distributions overlap such that some in the placebo group did better than those in the hyperthermia group. At 6 weeks, the Cohen's d effect size between the groups was 1.66. At this value, about 40% of the two groups overlap. And remember, this is using the 4.27 Hamilton score difference, which is questionable given the large confidence intervals.

Finally, the placebo effect was greater for the hyperthermia group than placebo group. After the study, 94% of the hyperthermia group guessed correctly that they were in the experimental group, whereas only 71% of the placebo group thought they were receiving the experimental treatment. This would have artificially reduced the hyperthermia group's scores on the Hamilton based on the placebo effect alone.

Linguistic gymnastics are used in this and many other studies to give a medical model impression. More over, the very statistics reported ostensibly to justify a claim of superior treatment demonstrate the unconvincing nature of the results. Trivial effects, excessive confidence intervals, nomothetic washing away of individuality, and the placebo effect make this study of questionable use, other than to demonstrate that warmth can help some people feel better. How surprising is this?

"...SSRIs work. They may not work for every patient, but they work for most patients. And it's a pity if their use is discouraged because of newspaper reports."

"The finding that both paroxetine and citalopram are clearly superior to placebo...when not producing adverse events, as well as the lack of association between adverse event severity and response, argue against the theory that antidepressants outperform placebo solely or largely because of their side effects...."

"...our results indirectly support the notion that the two drugs under study do display genuine antidepressant effects caused by their pharmacodynamics properties."

"And we did have an impressive, robust difference between active drug and placebo...."

These statements sound impressive. But the effect sizes between the SSRI and placebo groups in the study demonstrate that the difference between the groups is nearly meaningless. The reported effect sizes ranged from .31 to .49. See the graphic representation below which shows an effect size of .5:

The dark blue group would represent the people who took the SSRIs. The light blue represents the placebo group. One can see that the average level of depression for the SSRI group is less than that of the placebo group.

But look at how much the two groups overlap. Given the range of effect sizes in the study, 80-88% of the two groups would overlap. This means many people in the placebo group did better than people in the SSRI group, and many people in the SSRI group did worse than the people in the placebo group! With this in mind, how could the above claims of SSRI superiority be justified? They can't.

This bold sounding announcement that the question has been finally settled about SSRIs' superior effectiveness is typical of those who continue to support the medical model of human suffering. They use statistics to obscure practical and clinical significance. Looks good in medical journals and unless one understands the basics of statistical analyses (in most cases, the effect size is the telling number), it sounds good in media reports too.

The article mentions Irving Kirsch, Ph.D., who has critiqued the use of SSRIs (as have many others). Dr. Kirsch rightly points out another little known issue with studies like these. Not only is a placebo effect likely just because someone knows they are taking a substance (and they think it is the SSRI), but also because those taking the real SSRI will notice the psychoactive effects of the real chemical, and this will enhance the placebo effect. So, one would expect a small effect size difference between the SSRI and placebo group based on this alone. This is exactly what the study shows. Dr. Kirsch cautions that we should weigh this small, meaningless, effect with the potentially harmful side effects of taking these and other drugs to quell human emotional struggles, typically in combinations with other psychoactive drugs.

These above issues make this announcement weak. The study is far from demonstrating that SSRIs, or any other psychoactive drug, is an effective way to address the meaning-laden and personal struggle we call depression.

Religion – Is It All In The Brain?

A recent study in Neuropsychologica about veterans and brain trauma is a prime example of how medical model thinking and nomothetic research design and analysis wrongly imply: (1) that meaningful human experiences can be best understood by looking at the brain; and (2) that differences between research groups as identified by statistical tests, mean that the class of people in one group share a common characteristic different from the class of people in the other group(s). Unfortunately for the authors of the study, this is not true.

First, the follow quotes from the study reveal how meaningful human experiences are falsely reduced to brain structures:

“…religious beliefs are critically represented in the anterior frontal lobe.”“…fundamentalist religious beliefs arise from the integrated processing and computations in a distributed brain network….”“…a vmPFC lesion induces increased fundamentalism.”“…religious beliefs are partially dependent on correct functioning of the PFC.”

None of these statements are accurate. We’ll never find religious beliefs inside the skull and brain activity does not give rise to religious belief, even though religious belief cannot happen without brain activity. Religious belief, in addition to a plethora of other kinds of meaningful human experiences, can only be understood by understanding the individual person, and even that changes over time. Further, given that they are individuals, people are inescapably nuanced, complex, and unique in terms of the factors that interact and lead up to any one particular characteristic, such as religiosity.

It is true that damage to an area of the brain necessary for a person to have a certain opinion, belief, conviction, or feeling can change the person’s experience of those things. However, especially in the case of highly meaningful things, like religiosity, such changes occur more often not because of damage to those areas but because of experiential changes in living. This study never takes this into account: that veterans who have suffered TBI had more severe and meaningful experiences (both during the trauma and post-trauma) than those who hadn’t suffered TBI. How did those experiences, and not brain damage, affect their turn toward religious fundamentalism?

Regarding the second issue, there was a statistically significant difference in fundamentalism scores between the group of veterans who suffered damage to the ventromedial prefrontal cortex and the group with damage to the prefrontal cortex but outside the ventromedial and dorsolateral regions. Yet, the Cohen’s D was only .71. This means the two group distributions of fundamentalism scores overlapped around 73%.

Given this amount of overlap of groups, it does not justify the researchers’ claim that, “…participants with vmPFC lesions reported greater fundamentalism.” or “[p]atients with vmPFC lesions scored higher in fundamentalism than patients without PFC lesions….” Neither of these claims represents the data. In fact, a large number of people in the ventromedial group had lower fundamentalism scores than the other group, and vice versa, contrary to the claim. If damage to that region increases religious fundamentalism, it should apply to all of them.

Moreover, the amount of variance in the data explained by the ventromedial lesions was only 1%. That means 99% of the observed variance in fundamentalism data among the participants was due to something other than the lesions. In fact, this study found that openness (9.7%) and cognitive flexibility (4.6%) explained far more variance in the data than did the lesions. This suggests a person’s subjective understandings of the world, separate from brain injury, are more important in understanding religiosity. And note that even with all of the studied variables included, only about 18% of the variance was explained; 82% was unexplained. This is the important statistic. Much of what people do can't be explained by using medical model, nomothetic approaches. It is important to understand one person at a time.

Despite the above, the “moral of the story” according to the authors is how damage to brain structures affects one’s religious fundamental beliefs. This perpetuates a medical model of humanity that reduces meaningful experiences to sterile brain activity, and it stereotypes people without even a minimal amount of justifying evidence.

ADHD Causes Car Accidents?

The results of a study, published in JAMA Pediatrics, claims that ADHD causes an increased risk of automobile crashes. I'll explain why this is a trivial conclusion. What's more, it is absurd that the authors suggest more research into “the specific mechanisms by which ADHD influences crash risk to develop effective countermeasures.” ADHD is not a disorder that causes anything. ADHD is a label that describes a constellation of behaviors. To say it is a disorder that causes an increased risk of crashes is like saying walking is a disorder that causes an increased risk of moving.

If we look at the definition of ADHD contained in the DSM, we find that it consists of an arbitrary checklist of items about not paying attention and not inhibiting impulses. It has nothing to do with brain dysfunction. There are no laboratory tests to detect it. It has nothing to do with pathology in the person. It describes people who do not pay attention, not people who can’t. It is written in the language of medicine and to the untrained eye, it seems to be talking about a brain disorder, when in fact there is nothing mentioned about the supposed disorder and no medical evidence ever presented that demonstrates its pathological basis, and thus why there is no lab test for it.

And yet the announcement of this study will worry parents of children who have been labeled with this mythical disorder. They will fear when their children start to drive and wonder if driving privileges should be contingent on their children being in psychiatric “treatment” consisting of daily stimulant drug doses. The already bloated departments of motor vehicles across the country might even see this and similar studies as reason to implement new rules and programs about monitoring or denying driver’s licenses to people “with ADHD”.

But if we brush away all the medical-sounding and misleading language, we are left with a trivial study. In short, its results are saying that people who don’t pay attention while driving are at increased risk of having accidents. Aren’t we already able to make that assumption? When we don’t pay attention, we don’t notice things. It doesn’t take a scientific study to tell us this. And it doesn't need the creation of a disorder.

In addition, there are basic statistical issues with this study that further trivialize it. When comparing the driving records of people “with ADHD” and people who have not been given that diagnosis, the study concluded, “…the crash hazard among newly licensed drivers with ADHD was 36% higher.” In the first place, this is inaccurate. The wording makes it sound that people “with ADHD” are more dangerous on the road than people without that diagnosis. But the statistics used in studies like this one are based on group averages, not individuals. In this study, the average number of accidents for the group of ADHD people was claimed to be 36% higher than the average number of accidents in the non-ADHD group. Graphically, this would look something like the following display of two normally distributed (bell curved) groups. The horizontal axis represents the number of accidents and the height of the curve is the number of people with that number of accidents. The dark group would be the people without a diagnosis of ADHD and the lighter color group would be those “with ADHD”.

One can easily see with this graphical representation that even though the average (indicated by the vertical line) number of accidents of the ADHD group is higher than the non-ADHD group, many people in the ADHD group have less accidents than many people in the non-ADHD group. The reverse is also true: many people in the non-ADHD group have more accidents than people in the ADHD group. The reason the researchers say there is a 36% increased crash hazard among ADHD drivers is only because the average number of crashes is higher than the average number of crashes for the non-ADHD group. Still there a many ADHD people with less accidents than people with no diagnosis.

This is because the 36% increased risk of accidents is minimal. As an example, ADHD males in this study had a 13% risk of having an accident within 6 months after getting their driver's license. On the other hand, non-ADHD males only had a 9% risk. Even though this is only a 4% absolute difference in risk, the relative difference is a 44% increased risk when compared to non-ADHD males. Using the relative difference in risk makes it sound more important than it really is.

As an aside, it is interesting to note that the researchers had the diligence to test whether stimulants prescribed to the ADHD people had any effect on accident risk. One might think that taking a daily dose of Ritalin, which is chemically similar to cocaine, could negatively affect driving skill. But, the researchers found that it didn’t. But this begs the question, then, of what value are the stimulants? If those ADHD people who were prescribed stimulants had the same accident risk as those who hadn’t been prescribed stimulants, but who were still diagnosed with ADHD, that suggests the conventional stimulant drug treatment is useless in increasing attention and, in this study, in reducing accident risk. This is not good news for the advocates of drug treatment.

In short, this study is trivial because it is saying that people who don't pay attention while driving are at a higher risk of having accidents. This is a "duh!" conclusion. Nonetheless, the authors mislead away from this simple fact of life and give the impression that a disorder called ADHD causes those accidents. Recommending further study to identify the "specific mechanisms by which ADHD influences crash risk" is absurd. It is absurd because there are no mechanisms of ADHD. It is tantamount to saying we want to find the specific mechanisms of inattention. What would those be? Inattention is inattention and it can be problematic. But even worse, the authors talk about developing "countermeasures" to this inattention. Those so-called countermeasures are very likely going to be just further authoritarian and inhumane attempts at control, not because they would be focused on reducing accidents, but because they would be focused on "treating" a mythical disorder.

The Latest In A Long Line of Bogeymen?

A recent article in Health News From NPR asks the question: "Is 'Internet Addiction' Real?" Other than the possible minimizing effects of using quotes around the term, this article does nothing but reify a concept in a very misleading and potentially dangerous way. It adds to a long line of others that perpetuate the myth of mental illness, and in particular the recent technological phenomenon of social media over the Internet.

This article is an example of how mental health professionals are notorious for over-complicating human behavior. Instead of focusing on real life problems teens face in an increasingly compliance oriented and superficial world, they obsesses about what is the correct “disorder”. Then the “disorder” is the focus of investigation instead; meaning that something is wrong with the teen. To quote the DSM, it is “…a dysfunction in the individual.” It is the dysfunction “in” that causes the behavior. And this leads to meaningless questions as posed in the article, like “when does an obsession become an addiction?” Would it be better to think of these professionals having a “diagnosis addiction”?

In actuality, there is no dysfunction “in the individual”. There is a challenge over how, when, why, and to what extent technology is used and what things are considered popular and of value to teens. Internet and other IT technology is going to stay with us and probably get even more complex. My great grandmother once told me how terrible the invention of the telephone was. Up until then people would write letters to each other. After the telephone, she feared they wouldn't write to each other anymore. Instead, they would become impersonal and spend too much time on the telephone. Her fears panned out. But was that an addiction at work?

Much of the description of Naomi’s behavior in this article is attributed to her “addiction” to the internet. But it actually just describes typical teen turmoil in their attempts to navigate that line between separation and belonging. But once a scapegoat like “addiction” is identified all sorts of problems can be attributed to it. The article actually points this out when it notes she also had to deal with how to become popular among her peers, how to cope with her parents’ discord, how to handle less then perfect academic performance, and how to cope with the death of her grandmother. These are all quite typical challenges of adolescence.

The overall flavor of this article reminds me of the alarmist quality of “Reefer Madness”, a 1930’s film that demonized marijuana, and implied that it led to all sorts of antisocial and dangerous behaviors. The psychologist at her $10,000 a week “treatment” facility said, “these teens are using smartphones and tablets…for the same reasons others turn to hard drugs - to numb what is really going on inside.” Really? Is that what doctors in the 1800’s would have said about my great grandmother’s prediction about telephone use?

The problems facing teens are significant and they can be very serious. But it is not because they “have” an “addiction” to anything. It is because they are faced with the most difficult set of social circumstances any teenagers throughout history have had to face before now. They struggle with the means of instantaneous gratification, the ever-increasing demand of consumerism, the age-old longing to belong, and how to meet parental expectations.

The term “addiction” is merely short hand for “a strong urge to do something because that something is enjoyable in the short term, but causes problems in the long term.” There is no need to reify it as if it is an entity that invades people and causes them to do things. In fact, it could easily be argued that talking about it and treating it as if it were some alien entity calling the shots is harmful and perpetuates the problem.

ADHD? A Food Deficit?

On April 9, 2017, an article appeared on the website, “The New American”. The writer, Joe Wolverton II, J.D., tells the story of a seven-year-old boy who was taken away from his family by Child Protective Services because his school decided he was “mentally unstable”. The parents of Cameron Maple, of Lebanon, Ohio, were instructed to take him to a hospital so that his disorder could be diagnosed. When the parents demurred, the state stepped in and placed the child in protective custody, citing “health neglect” against the parents, since they would not comply with the psychological evaluation recommended by the school administration.

This situation is wrong on many levels. There is no such thing as “ADHD” as a literal neurobiological disease that can be diagnosed and treated. With this in mind, it is regrettable this child was ripped from his parents’ home because a nonexistent “ADHD” was suspected. I think that something else could be going on. There could be a real bodily dysfunction that is being overlooked in many of these unfortunate children who are being labeled “mentally ill”. They could simply be malnourished.

There are many books out there written on the topic of “ADHD”, but as a Nutritional Therapy Practitioner and a Gut and Psychology Syndrome (GAPS) Practitioner, I have a different take on a possible answer to the question, “What is ADHD?” We know that a child’s brain requires nutrient-dense foods for proper development. This means things like eggs, cod liver oil or other fish oils, butter, liver, beef, lard, and a host of other fatty foods. The brain, of course, is largely made up of fats. When the proper fats are lacking or deficient, the brain does not function properly. We would say the child is malnourished.

How does a child with these nutritional deficiencies behave? They are not able to manage their behavior very well, and are apt to appear fidgety and unfocused. They lack the self-control they need to fit into social situations, like school, effectively. They have trouble controlling their moods, as well, and often seem inappropriate in their responses to the environment.

Children who are properly nourished, are much more able to control their behavior, to stay on task, and they suffer less from negative moods, like anxiety and anger. Their bodies can create the neurotransmitters their brain needs to calm themselves down and be happy, because they are eating the proper amino acids and other micronutrients their bodies need to do so.

A study done in Norway in 2013 showed that children who ate a diet largely consisting of processed sugary foods, and lots of starches like bread and buns, pizza and the like, were far more apt to exhibit either internalizing behaviors like worry, sadness and anxiety or externalizing behaviors like tantrums, hyperactivity and aggression.

On the other hand, children who ate lots of cheese, fish, vegetables and eggs showed fewer such symptoms. The point is, a child’s diet affects behavior and moods, either for good or ill, and diet is an important factor in this.

Another thought is that when a child develops his or her own diet, choosing starchy and sugary foods over anything else, it is likely that they are suffering from small intestinal bacterial overgrowth (SIBO). We know that if candida albicans, a fungus/yeast, takes over the small intestine, it is capable of sending messages to the brain instructing the person to eat more sugar and starch, its favored foods.

Thus, you have children who will preferentially eat these foods, to the exclusion of the healthier vegetables, meats, eggs, yogurt and other raw and fermented foods. This becomes a vicious cycle, eating the wrong foods, and being reinforced from the gut to continue to do so. Many parents despair of ever seeing their children take a bite of a vegetable. This is gut dysfunction, and when this situation continues for too long, intestinal permeability, or “leaky gut” appears. Toxins, produced by bacteria, or other toxic wastes, can leak into the bloodstream, and past the blood-brain barrier and into the brain, causing disordered thinking.

If some of you recall, ADD or ADHD used to be called “Minimal Brain Dysfunction”. It would be wonderful to get back to that concept, and apply the cure: Proper nutrition and healing the gut. Then, we could look forward to complete remission of that real dysfunction!

Elizabeth Szlek is the Director of The Door Counseling Center of Yorkville, NY. She is a Licensed Mental Health Counselor, a Nutritional Therapy Practitioner and a Certified GAPS Practitioner. She can be reached at (315) 768-8900 or at door@thedoorcounselingcenter.com.

Ms. Stahl interviewed producers and cast members from Sesame Street. She also spoke to parents with autistic children, and others who love them. It was an emotional segment, in a good way. Sesame Street intends to de-stigmatize children with autism, and everyone is proud.

I started watching 60 minutes and Sesame Street in the 1960's. Like most Americans, I learned to love, and trust, both shows. Coincidentally, during the same decade, I first became interested in autism.

Lloyd Nolan, a character actor from the 40’s, 50’,s and 60’s, was on the Johnny Carson show. He spoke of his “strange” 4 year-old son who had something called “autism.” I was captivated as he described in some detail the very odd behaviors of his son, Jay – and I’ve been captivated since.

Fifty years later, autism, Sesame Street, and 60 minutes converged in mid-March, 2017, with one reviewer of the show saying: “Sesame Street’s new Muppet Julia brought 60 Minutes viewers to tears.”

Brought me to tears too. For different reasons.

It’s Not So Easy Being Mean

Dear parents and other caretakers who love and protect and cherish these very unique children, I love them too.

For me, it’s a matter of temperament (See Keirsey’s brief portrait of this temperament in Notes). There is no biology to this, or genetics. These kids aren’t flawed or damaged. They aren’t disabled or disturbed or diseased either. That means they don’t need doctors, or their medicine. They do need our protection, because they are unique, and because they are so terribly misunderstood, and because someone is always trying to fix them. Some of their famous counterparts include Mozart, Spielberg, Cher, and Harpo Marx. There is much more about this, for a different place and time.

For now, parents and caretakers, and others who love these children as I do, please consider the following:

In 1983, the autism rate was 4.3 in 10,000

I know this is accurate. I was 38, in the profession for nearly 10 years, and I was in the final year of my Masters program (I received my Ph.D. about 4 years later). In the next 12 months I researched everything known at the time about autism, beginning with Leo Kanner. My research included Hans Asperger. I also did a year internship as a family therapist for 6 families with autistic kids (all boys). My Master’s thesis was titled: Autism and Other Self Defiling Phenomena. I was as informed about this very small population as anyone was at the time. Again, the incident rate was 4.3 in 10,000.

Keeping it simple, this means if there were 10,000 children randomly gathered in a large auditorium, we could expect to find 4 or 5 children who fit the description of autism in 1983.

In 2017, the autism rate is 1 in 68

Doing the math, that means the same auditorium with 10,000 randomly gathered children would now have about 150 children who fit the evolving, all inclusive description of autism. That’s an increase of 3500% - in 34 years.

How did that happen?

Is autism contagious? If so, how so? If not, how does it “spread?” Is there a virus or bacteria? Did something drastic happen to our water system in the last 4 decades? In the last 34 years, did the mercury just suddenly appear in the fish these children or their parents ate, that wasn’t there before? Did someone change the formulae for vaccines? Was there some other environmental catastrophe that triggered this incredible spike in the number of diseased children in that auditorium? By the way, these are some – not all – of the speculated “causes” of autism.

I’ve asked medical professionals who should know how this “epidemic” occurred, many, many, many times. They usually duck the question, or provide some form of psychobabble. I’m skilled at recognizing psychobabble.

So, can anyone from medicine explain this “epidemic,” please? Short answer? No. No one can. Long answer? No.

No one can.

So what really happened?

Psychiatry Happened

I’ve been awestruck, and demoralized, as the rate of autism has skyrocketed, without much fanfare. It’s been dramatic.

Why the "epidemic?” Because there has been an epidemic of diagnosers, armed with an ever-widening, all-inclusive diagnosis - nothing else.

The Psychiatric Process: Change the Definition

Autism was added to the 1980 edition of DSM III (Diagnostic Statistical Manual). This made it official. Autism became medical. It was called Infantile Autism disorder back then. There were six characteristics listed and each of the six had to be present to be diagnosed. Doctors mostly ignored what was then a very, very rare phenomenon. (See what Leo Kanner had to say about the rarity of autism in Notes)

By 1985, the rate was 1 in 2500.

In 1994, the DSM definition of Autism changed again, significantly. This is when I first became concerned. I knew what was coming. After a forty-year career – the last 25 as director of several mental health facilities for children - I’ve seen psychiatry do this as a matter of course.

Now there were 16 different symptoms, and only six of the 16 were needed to receive the diagnosis. As a result, the universe of diagnosable children grew exponentially. The game was officially rigged. The "epidemic" started.

By 1995, the rate was 1 in 500.

Enter ASD: The Final Solution

In 2013, DSM V was released. The diagnostic criteria for autism included these instructions to all professionals: "Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive developmental disorder (PDD) should be given the diagnosis of autism spectrum disorder."

There you have it. They "lumped" together all the symptoms of Asperger’s and PDD with "autism," and the population's diagnostic horizon multiplied - again. Now, any child who is a little too quiet, a little too distracted, a little too defiant, a little too introverted, can be on the “spectrum.” Also, because he can speak, doesn’t mean he isn’t on the “spectrum.”

By 2016, the rate is 1 in 68.

The Rest Is Easy for Psychiatry

Psychiatric scientists will argue for years, in the right journals, with academic vigor, about scientific studies that expose the real cause of autism. Is it genetic? There’s some “convincing” evidence. Is it the vaccine? Studies show a “link.”

What about a chemical “imbalance” in the brain? “There’s a correlation,” says the psychiatric scientist. By the way, psychiatry will neither offer, nor promise any cures. There’s a good reason for this. Psychiatry has a perfect record in this regard – 0 cures.

Will psychiatry ever find a “cause?” No, they won’t, for two reasons: (1) they never have, for any of the more than 400 disorders in DSM V and, (2) autism isn’t a disease, so a medical cause can never be found.

In the meantime, psychiatry will eagerly “treat the symptoms” with a variety of chemicals. Here’s what they’ve tried so far with these children:

Finally, psychiatry will caution all of us routinely, in eye-popping, fear invoking headlines, that the “epidemic” is worsening, again.

This is what the psychiatric medical model has to offer humanity, and it's 2017.

One More Thing to Consider

In 1957, Hollywood released "The Three Faces of Eve.” Based on a true story, the movie is about a young woman with three personalities. Joanne Woodward won an Academy Award for her portrayal of Eve. For a few years afterwards, there was a short-lived “outbreak” of multiple personality disorder reported by psychiatrists in America. A small industry was born, and then faded away. The “outbreak” ended.

If this movie was made in 2007 instead of 1957, there would be multiple personality websites, multiple personality theories, multiple personality medications, a slew of multiple personality books, multiple personality experts, and endless studies among medical professionals searching for the cause that would include genes, brain damage - maybe even vaccines - and a huge epidemic would still be growing. And, as usual, psychiatry would be ready to supply the chemicals, to treat the symptoms, while they look for the ever-elusive cause of multiple personalities.

This is, as far as I'm concerned, the genesis of modern day psychiatric "epidemics."

Like I Said – It’s not so easy being mean

The people at 60 minutes, and the actors and crew at Sesame Street, and the parents and professionals who know these children have unquestioned love and honest and pure intentions. They are assertively protective of these children, and they make sure they are informed.

From my perspective, it is a gut wrenching experience watching this tragedy unfold. I’ve known for forty years – as do many, many others – these kids need good teachers, not doctors. There isn’t a deficiency or – forgive us all – a “handicap.” (See what Hans Asperger had to say about “cure” in Notes.)

I’ll Be Watching Too

How will they portray Julia on Sesame Street?

Will she be unresponsive? Will she avoid eye contact? Will she be off to herself, isolated? Will she be portrayed as socially inept? Will she have difficulty making friends? Will she be fixated on an unusual object? Will she engage in various rituals? Will she become expressionless? Will she use peculiar phrases? Will she lack an interest in making friends? These are just some of the “symptoms” of children on the “spectrum.”

Will adults – professional and otherwise – be defending her behavior by explaining to everyone that Julia has a brain disorder and needs our understanding about her “challenges?”

Not without hearing from me, for what it’s worth.

Finally

To Ms. Stahl, to Oscar, to Big Bird, and all the others at Sesame Street, and to the parents and caretakers of these very special kids – we are on the same side. I love these kids too. I want to protect them too.

Lastly, dear Julia, your debut is loved and protected, and that’s a good thing. I can already tell, you’re going to be great. Everyone is watching.

Just be yourself.

~~~~~~~~~~~~~~~~~~~~~~~~~~Notes

Kanner believed, and argued over his lifetime, that autism was rare. He must have noticed an initial “outbreak.” The John Hopkins psychiatrist “undiagnosed” – and sent home – 9 out of 10 children sent to his practice by other clinicians.

Asperger believed the "cure" for the most disabling aspects of autism is to be found in understanding teachers, accommodating employers, supportive communities, and parents who have faith in their children's potential.

Many people have read or are familiar with Kanner’s first 11 cases of autism. Less well known is the 30 year follow up for those 11 cases. Note the outcomes for the children left in hospitals. You can read it here. ~~~~~~~~~~~~~~~~~~~~~~~~~~

“Autism” from another point of view

“Composers are just as plentiful as the other Artisans, say nine or ten per cent of the population, but in general they are very difficult to observe and thus greatly misunderstood. Very likely the difficulty comes from their tendency not to express themselves verbally, but through their works of art. Composers are usually not interested in developing ability in public speaking, or even in the art of conversation; they prefer to feel the pulse of life by touch, in the muscles, in the eyes, in the ears, on the tongue. Make no mistake, Composers are just as interested as other types in sharing their view of the world, and if they find a medium of non-verbal communication-some art form-then they will express their character quite eloquently. If not, they simply remain unknown, their quietness leaving their character all but invisible.” Keirsey - (Please Understand Me II)

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